NagZ is required for beta-lactamase expression and full pathogenicity in Xanthomonas campestris pv. campestris str. 17

Abstract

Xanthomonas campestris pv. campestris expresses a chromosomally encoded class A β-lactamase Blaxc. Basal expression and induction of blaxc require the transcriptional factor AmpRxc and the peptidoglycan-monomers permease AmpGxc. NagZ is a β-GlcNAcase which cleaves GlcNAc-anhMurNAc peptides (peptidoglycan-monomers) to generate anhMurNAc-peptides. In many bacteria, anhMurNAc-peptides act as activation ligands for AmpR. Nevertheless, the role of NagZ in β-lactamase induction differs among species. In this paper, we studied the roles of nagZxc in the regulation of blaxc and pathogenicity in X. campestris pv. campestris. Our data showed that cells lacking nagZxc dramatically reduced the basal expression and induction of blaxc, suggesting that anhMurNAc-peptides, products of NagZxc, are required for blaxc expression regardless of the presence or absence of inducers. Expression of blaxc is regulated via an ampG-nagZ-ampR pathway. Pathogenicity assay demonstrated that an ampGxc mutant excited more severe symptoms than the wild-type; on the contrary, the nagZxc mutant became less virulent. To our knowledge, this is the first demonstration of a link between the ampG or nagZ defects and the pathogenicity in a plant pathogen.

Keywords: Antibiotic resistance; Beta-lactamase; Bla; Pathogenicity; ampR; nagZ.